作者: Diletta Edifizi , Björn Schumacher
DOI: 10.3390/IJMS18112329
关键词:
摘要: DNA damage causally contributes to aging and age-related diseases. The declining functioning of tissues organs during can lead the increased risk succumbing aging-associated Congenital syndromes that are caused by heritable mutations in repair pathways cancer susceptibility accelerated aging, thus underlining importance genome maintenance for withstanding aging. High-throughput mass-spectrometry-based approaches have recently contributed identifying signalling response networks gaining a more comprehensive understanding physiological adaptations occurring upon unrepaired damage. insulin-like pathway has been implicated (DDR) network includes epidermal growth factor (EGF)-, AMP-activated protein kinases (AMPK)- target rapamycin (TOR)-like pathways, which known regulators growth, metabolism, stress responses. same together with autophagy-mediated proteostatic decline energy metabolism also found be similarly regulated natural suggesting striking parallels adaptation persistent due defects long-term low-level accumulation These insights will an important starting point study interplay between involved progeroid deficiencies gain new consequences process.